Multiparametric monitoring of the awake brain exposed to carbon monoxide

• Published in: Journal of applied physiology (1985) Vol. 78; no. 3; p. 1188
• Main Authors: Mayevsky, A, Meilin, S, Rogatsky, G G, Zarchin, N, Thom, S R
• Format: Journal Article
• Language: English
• Published: United States 01.03.1995
• Subjects: Animals; Brain - drug effects; Brain - metabolism; Carbon Monoxide - pharmacology; Cerebrovascular Circulation; Extracellular Space - metabolism; Ions; Mitochondria - metabolism; Monitoring, Physiologic - instrumentation; Monitoring, Physiologic - methods; NAD - metabolism; Oxidation-Reduction; Rats
• ISSN: 8750-7587
• DOI: 10.1152/jappl.1995.78.3.1188

We have applied in vivo real-time techniques to monitor the physiological changes associated with exposure to a pattern of carbon monoxide (CO) known to cause brain oxidative stress. Using a multiparametric monitoring device connected to the brain, we exposed unanesthetized rats to two levels of CO, 0.1 and 0.3% in air. Energy metabolism was evaluated by the optical monitoring of relative cerebral blood flow (CBF) and intramitochondrial redox state. Ionic homeostasis was assessed by measurements of K+,Ca2+, and H+ or Na+ levels in the extracellular space. The electrical parameters monitored were the electrocorticogram and direct current steady potential. Under 1,000 ppm of CO, the CBF was increased significantly without any measurable change in the NADH redox state, suggesting that the cause for the increased CBF was not hypoxia. Exposing the awake rat to 1,000 ppm of CO (40 min) followed by 3,000 ppm of CO (20 min) led to an increase in CBF followed by episodes of spontaneous brain depolarizations characterized by changes in ionic homeostasis and blood flow. These changes were similar to those recorded under cortical spreading depression. In most animals exposed to 3,000 ppm of CO, spontaneous oscillations in CBF and NADH redox state that were negatively correlated were recorded. The results indicate that an inspired CO level of 0.1% had effects largely restricted to blood flow, whereas at a higher CO level an additional impairment in energy supply resulted in a complex pattern of effects similar to that caused by brain ischemia.